Derm (Atopic Dermatitis) Flashcards
Define allergic contact eczema (dermatitis)
A red, itchy, weepy reaction where the skin has come into contact with a substance that the immune system recognises as foreign, such as poison ivy or certain preservatives in creams and lotions
Define atopic dermatitis
A chronic skin disease characterised by itchy, inflamed skin.
It is a chronic, system, relapsing, inflammatory disease- not a localised skin condition
Define contact eczema (dermatitis)
A localised reaction that includes, redness, itching, and burning where the skin has come into contact with an allergen (an allergen-causing substance) or with an irritant such as acid, cleaning agent, or other chemical
Prevalence of AD
15-30% of children, 1-3% of working adults
Role of filaggrin in allergic skin disease
Mutations in filaggrin gene lead to filaggrin deficiency that leads to impaired barrier function and enhanced allergen exposure.
Environmental RFs for AD
Air pollution, increased infant washing, increased water hardness, high latitudes
Protective environmental factors for AD
Increased UV light exposure and increased outdoor temperature, increased humidity
Pathophysiology of AD
- Defects in skin barrier lead to penetration by antigens, which encounter Langerhans cells (a type of dendritic cell found in skin), which activate T helper 2 (Th2) cells.
- Th2 cells release cytokines IL-4, IL-5, and IL13. IL4 increases Th2 survival. These cytokines also drive lgE synthesis by B cells and recruitment of peripheral eosinophils but these cells are thought to be by-products of Th2 activation rather than pathogenic mediators of AD.
- Th2 cytokines disrupt the skin barrier function by inhibiting expression of filaggrin (a protein essential for skin barrier formation) and antimicrobial peptides (the first-line defence against infectious agents). This results in enhanced penetration of allergens and pathogens.
- Allergens and pathogens cause epithelial keratinocyte damage, leading to release of IL33, IL25 and TLSP. They activate both dendritic cells and group 2 innate lymphoid cells (ILC2) to drive the Th2 inflammatory responses.
- In chronic AD, TH22 cells release IL22 which induces thickening and discolouration of the skin. TH1 cells produce reduced lvls of IFN-y, a cytokine which suppresses. Th2 inflammation.
Epidemiology of AD
Prevalence in caucasian population is higher than asian.
Clinical phenotypes:
- Asian: well demarcated erythematous plaque-like lesions
- Caucasian: ill-defined flatter erythematous skin lessions
Typical distribution of AD
cheeks, elbow (front and back), write (front), behind knee. groin area not affected
Clinical features in diagnosis of AD
Essential features (must be present):
- pruritis
- eczema (acute, subacute, chronic): flexural lesions, sparing of groin and axillary regions, chronic or relapsing hx
Important features (seen in most cases, supports the diagnosis of AD):
- early age of onset
- atopy (genetic tendency to develop allergic diseases?): personal/family hx (of AR or asthma), lgE reactivity
- xerosis (dry skin)
Major and minor S&S of AD
Major indicators:
- pruritus (intense itching)
- characteristic rash in locations typical of disease
- chronic or repeated occurring smx
- personal or family hx of AD (eczema, hay fever, asthma)
Selected minor indicators:
- early age of onset
- dry skin that may also have patchy scales or rough bumps
- increased serum lgE
- numerous skin creases on palms
- hand or foot involvement
- inflammation ard lips
- nipple eczema
- susceptibility to skin infection (bacteria): superficial (epidermis, dermis) or non-superficial -> as itching may cause broken/excoriated skin)
- positive allergy skin tests
Clinical presentation of AD in an infant
Red, if touch and it blanches, it is erythematous. Lichenification (hardness). No excoriation so less risk of infection
Extensor pattern of AD
well defined, lichenfication
Clinical presentation of AD in the popliteal fossa (behind knee joint)
skin lesions, papules, excoriated
Hx taking: specific questions to ask patient
- Is itching present?
- distribution of rash
- fam hx of atopy
- how freq they wash their skin
- what type of water they use to wash?
Measures of AD severity
SCORAD Score > 50: Severe AD
SCORAD Score 25-50: Moderate AD
SCORAD Score <25: Mild AD
Non-pharm therapy of AD
Identify any triggers.
- prevent overshowering
- reduce stress
- food hypersensitivity: egg, milk, wheat, fish, soya -> avoid
- remove allergens (house dust mite, animal dander, moulds/pollens, cosmetics (contains preservations)
Baseline: basic therapy for AD in adults
Educational programmes, emollients, bath oils, avoidances of clinically relevant allergens.
How does Complete emollient therapy help?
emollient therapy is cornerstone of management of AD and acts through maintenance of skin barrier. It forms oclusive later, reduce water loss and exposure to bacteria.
It improves smx of itch, pain, prolong time to a flare up, reduce potency and amt of CS used to control AD.
It is used for all types (mild, mod, sev AD).
For inflamed areas or those with genetic predeposition to AD and wishes to prevent it: lotions
For dry skin: ointments.
Example: suu balm menthol cream used BD-TDS everyday. Physiogel DMT cream.
Ceramides (works as emollients?): re-inforce skin barrier and increases hydration
MILD: SCORAD <25 or transient eczema therapy
Reactive therapy with topical GCS class II or depending on local cofactors: topical calcineurin inhibitors, antiseptics incl. silver/silver coated textiles.
MODERATE: SCORAD 25-50 or recurrent eczema
Proactive therapy with topical tacrolimus, or class II or class III topical GCS, wet wrap therapy, UV therapy, psychosomatic counseling, climate therapy
SEVERE: SCORAD >50 or persistent eczema
hospitalisation, systemic immunosuppression, cyclosporine, short couse of OCS, dupilumab, MTX, azathioprin, PUVA, alitretinoin, mycophenolate mofetil
Least potent topical CS used in AD
hydrocortisone 1%, 2.5% in cream, lotions or ointments
